Economic Discrimination is as bad as Racial Discrimination [says ChatGPT]

Radio 4 mentioning huge studies linking discrimination with inflammation and poor health. So I asked ChatGPT to compare these results with the ones for economic deprivation. And they are the same. So when Socialists say that an unequal society is a crime it is on the same level as racism. Capitalism is effectively racist. Now capitalist proponents say everyone can skill up, get a job (employment from a capitalist, or borrow to start a company from a capitalist), work hard and get rich so it is discrimination they bring on themselves. But this isn't Capitalism this is true everywhere even in a dictatorship you can work to get favour in the system and become successful. Famous examples are Abdul Karim a Muslim getting into the inner circle and confidence of Queen Victoria. Capitalism by contrast is the system of "capital" where the more you have the more you get via rent seeking from the poor.

#EndCapitalism

===

there are studies linking racial discrimination with inflammation. Are their similar ones linking economic deprivation with inflammation and which of the two racial or economic discrimination has the larger effect.

ChatGPT said:

Short answer: yes — there are many studies (and meta-analyses) linking economic deprivation / low socioeconomic status (SES) to higher systemic inflammation, and the estimated effect on common biomarkers (CRP, IL-6) is roughly similar in size to the associations reported for racial discrimination — both are small but statistically detectable on average. Which is “bigger” depends on the precise measure, biomarker, sample, and covariates — you can’t truthfully say one always outweighs the other.

Key evidence (brief):

• Socioeconomic status → inflammation. A large meta-analysis (43 papers, N ≈111,156) found lower SES associated with higher C-reactive protein (CRP) and interleukin-6 (IL-6): meta-analytic estimates were Z = 0.12 for CRP and Z = 0.15 for IL-6 (95% CIs reported). That is a small but consistent association across many studies. PubMed

• Racial / everyday discrimination → inflammation. A focused meta-analysis that pooled studies using the Everyday Discrimination Scale (k = 10 for CRP) found a pooled correlation with CRP of r = 0.11 (95% CI 0.01–0.20). The same meta found null/very small pooled associations for IL-6 and cortisol. Other recent syntheses report overall positive but modest correlations (for example one systematic review/meta-analysis reported pooled r ≈ 0.087 for discrimination and inflammation overall). MIDUS - Midlife in the United States+1

What those numbers mean (practically)

• Both SES and discrimination show small effect sizes on common inflammatory markers (CRP and IL-6). Small correlations (r ≈ 0.08–0.15 or Z≈0.12–0.15) are typical for population psychosocial → biomarker relationships: measurable at the group level and potentially meaningful for population health, but not “huge” at the individual level. PubMed+1

Important caveats and why direct comparison is hard

1. Different operationalizations: “SES” is measured as income, education, occupation or neighborhood deprivation; “discrimination” may be measured as everyday unfair treatment, major lifetime events, or institutional exposures. Different measures produce different effect sizes. PubMed+1

2. Different biomarkers and assays: CRP and IL-6 behave differently; some studies use blood, some saliva, and results vary by assay. Meta-analyses sometimes find CRP associations but weaker or inconsistent IL-6 findings. MIDUS - Midlife in the United States+1

3. Confounding and mediation: BMI, smoking, poor sleep, comorbidities and health behaviors (which are themselves patterned by SES and by experiences of discrimination) attenuate or mediate associations. Some adjusted analyses find smaller effects once BMI and behaviors are included. That complicates attributing net effects uniquely to SES vs discrimination. MIDUS - Midlife in the United States+1

4. Overlap and intersectionality: SES and racial discrimination are correlated (racialized groups are disproportionately exposed to economic deprivation and to discrimination). Their effects can be additive, multiplicative, or mediated by one another depending on context; some work attempts to partition how much of a racial difference in inflammation is explained by SES versus discrimination and finds both matter. ScienceDirect+1

5. Study design limits causal claims: most evidence is observational and many studies are cross-sectional, so reverse causation and residual confounding are concerns. Longitudinal and quasi-experimental studies strengthen causal inference but are fewer. MIDUS - Midlife in the United States+1

Bottom line (practical takeaway)

• Both economic deprivation (low SES) and racial discrimination are linked to higher inflammatory markers in the population, and the pooled estimates from meta-analyses put their typical effect sizes in the same small-to-modest range (roughly r/Z ≈ 0.08–0.15 for CRP/IL-6 in many pooled estimates). You should therefore think of them as both important and partially overlapping contributors to “getting under the skin.” Which is “larger” depends on the dataset, the marker, and what covariates are controlled for — there isn’t a universal answer that one is always stronger. PubMed+1

If you want next steps, I can:

• pull and summarize the exact effect sizes and confidence intervals from the most influential meta-analyses and show a small table comparing CRP and IL-6 estimates for SES vs discrimination (so you can see numbers side-by-side), or

• find longitudinal or cohort studies that attempt to separate the contributions of SES and discrimination (e.g., mediation or decomposition analyses), or

• summarize the primary mechanistic pathways (behavioral, HPA axis, sympathetic signaling, epigenetic/telomere work).

Which of those would be most useful to you?